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Belle Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Three steps of acute inflammation

A

Vascular: dilation of vessels
Exudative: vascular leakage of protein rich fluid
Cells recruited: neutrophil polymorphs

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2
Q

Causes of acute inflammation

A

Microbial infections e.g. bacteria
Hypersensitivity reactions e.g. parasites
Physical agents e.g. heat
Chemicals e.g. acid

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3
Q

Neutrophil polymorph emigration

A

Margination of neutrophils
Adhesion of neutrophils (pavementing)
Neutrophil emigration
Diapedesis (leukocyte extravasation)

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4
Q

Outcomes of acute inflammation

A

Resolution: complete restoration of tissues e.g. acute lobar pneumonia

Suppuration: formation of pus, leads to scarring

Organisation: replacement by granulation tissue, macrophages migrate, fibrosis occurs e.g. post-MI

Progression: causative agent is not removed, progresses to chronic

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5
Q

Cells involved in acute inflammation

A

Neutrophils: phagocytose pathogens
Monocytes: migrate to tissue and become macrophages which induce chemotaxis

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6
Q

Cells involved in chronic inflammation

A

Lymphocytes, macrophages, plasma cells

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7
Q

Macroscopic appearance of chronic inflammation

A

Chronic ulcer
Chronic abscess cavity
Granulomatous inflammation
Fibrosis

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8
Q

Cellular cooperation in chronic inflammation

A

B lymphocytes: plasma cells, antibody production
T lymphocytes: cell-mediated immunity
Macrophages: respond to chemotactic stimuli, cytokine production (interferon alpha and beta, IL1, IL6, IL8, TNF-alpha)

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9
Q

Granulomas

A

An aggregate of epithelioid histocytes (activated macrophages resembling epithelial cells)

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10
Q

Causes of granuloma development

A

TB (most common)
Leprosy
Chrons
Sarcoidosis

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11
Q

Granuloma and eosinophil presence

A

Parasite

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12
Q

Platelet alpha granules

A

Platelet adhesion e.g. production of fibrinogen, vWF

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13
Q

Platelet dense granules

A

Platelet aggregation e.g. ADP

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14
Q

First stage of thrombus formation

A

Platelet aggregation (starts the clotting cascade)

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15
Q

Three major causes of thrombosis (Virchow’s triad)

A

Reduced blood flow (stasis) e.g. immobility

Blood vessel/endothelial injury e.g. trauma, HT

Hypercoagulability e.g. smoking

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16
Q

Arterial thrombosis formation

A

Atheromatous plaque causes turbulence in blood flow
Loss of endothelial cells, exposure to collagen
Platelet adherence and activation
Thrombus: platelets > fibrin > RBCs
Grows in the direction of blood flow (propagation)

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17
Q

Venous thrombosis patho

A

Lower blood pressure in veins, atheroma do not occur
Thrombi begin at valves which produce a degree of turbulence and can be damaged e.g. stasis
Formed under low blood pressure
Mainly made of RBCs

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18
Q

Clinical features of arterial thrombi

A

Loss of pulse distal to thrombus
Area becomes cold, pale and painful
Possible gangrene

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19
Q

Clinical features of venous thrombi

A

Tender

Area becomes reddened and swollen

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20
Q

Complications of arterial thrombus and treatment

A

MI/stroke

Tx: anti-platelets e.g. aspirin

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21
Q

Complications of venous thrombus and treatment

A

DVT/PE

Tx: anti-coagulants e.g. warfarin

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22
Q

Pulmonary embolism

A

Venous emboli travel to vena cava and lodge in the pulmonary arteries

Presentation:
Acute respiratory or cardiac problems
Chest pain and shortness of breath

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23
Q

Ischaemic reperfusion injury

A

Damage to tissue during reoxygenation after a period of ischaemia

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24
Q

Atherosclerosis pathogenesis

A

High levels of LDL accumulates IN arterial wall

Macrophages and T-cells are attracted to the site of damage and take up lipid to form foam cells

Formation of fatty streak

Activated macrophages release cytokines and growth factors

Smooth muscle cell proliferation around the lipid core, thinning of tunica media

Formation of a fibrous cap (collagen)

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25
Q

Risk factors for atherosclerosis

A 
Hypercholesterolaemia (prevention: statins) 
Smoking
Hypertension
Diabetes
Male
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26
Q

Apoptosis

A

Programmed sequence of intracellular events leading to the removal of a cell without the release of harmful products to surrounding cells

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27
Q

Inhibitors of apoptosis

A

Growth factors
ECM
Sex steroids

28
Q

Inducers of apoptosis

A

Glucocorticoids
Free radicals
Ionising radiation
DNA damage

29
Q

Intrinsic apoptosis pathway

A

Mitochondrial pathway:
Biochemical stress e.g. free radicals
Bax: induces apoptosis (p35 cell cycle arrest)
Activation of caspase cascade

30
Q

Extrinsic apoptosis pathway

A

Used by the immune system to eliminate lymphocytes
Ligand binding at death receptors on cell surface
Receptors include TNFR1 (TNF-alpha ligand) and Fas receptor (Fas ligand)
Activation of caspase cascade

31
Q

Necrosis

A

Traumatic cell death which indices inflammation and repair

Characterised by bioenergetic failure and loss of plasma membrane

32
Q

Coagulative necrosis

A

Most common type
Can occur in most organs but most commonly heart and kidneys
Caused by hypoxia (ischaemia)

33
Q

Liquefactive necrosis

A

Hydrolytic enzymes

Occurs in the brain due to its lack of substantial supporting stroma e.g. stroke

34
Q

Caseous necrosis

A

Causes a cottage cheese pattern

TB is characterised by this form of necrosis

35
Q

Gangrene

A

Necrosis with rotting of the tissue

Affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)

36
Q

Fat necrosis

A

Fatty acids spill out of adipose cells

Pancreatitis

37
Q

Fibrinoid necrosis

A

Fibrin deposits

Vasculitis

38
Q

Hypertrophy

A

Increase in cell SIZE without cell division

E.g. muscle hypertrophy in athletes, uterine hypertrophy in pregnancy

39
Q

Hyperplasia

A

Increase in cell number by division (mitosis)

Cannot happen in cells that don’t divide i.e. myocardial cells or nerve cells

40
Q

Atrophy

A

Decrease in the size of an organ - can be a reduction in cell size or cell number
E.g. muscle atrophy in ALS

41
Q

Metaplasia

A

Change in the DIFFERENTIATION of a cell
Occurs in response to alterations in the cellular environment
E.g. squamous epithelium > columnar epithelium in Barrett’s oesophagus

42
Q

Dysplasia

A

Morphological changes seen in cells in the progression to BECOMING CANCER

43
Q

Carcinogenesis

A

Transformation of normal cells into neoplastic (cancerous) cells through permanent genetic alterations or mutations

44
Q

Why can neoplasms not arise in erythrocytes

A

No nuclei

45
Q

Tumour

A

Any abnormal swelling

46
Q

Carcinogen examples

A

Smoking - lung tumours
EBV - Burkitts lymphoma
HPV - cervical cancer
UV radiation - skin cancer

47
Q

Benign tumours features

A 
Do not invade basement membrane 
Exophytic (grow outwards)
Low mitotic activity 
Circumscribed (limited to an area)
Necrosis and ulceration are rare
48
Q

Malignant tumours

A 
Invade the basement membrane 
Endophytic (grows inwards)
High mitotic activity 
Poorly circumscribed 
Necrosis and ulceration are common
49
Q

Benign epithelial tumours

A

Papilloma (non glandular)

Adenoma (glandular secretory tissue)

50
Q

Malignant epithelial tumours

A

Carcinoma (malignant tumour of epithelial cells)

Adenocarcinoma (malignant tumour of glandular epithelial cells)

51
Q

Types of benign connective tissue tumours

A 
Lipoma: adipocytes
Rhabdomyoma: skeletal muscle 
Leiomyoma: smooth muscle cells 
Chondroma: cartilage 
Osteoma: bone
52
Q

Malignant connective tissue tumours

A 
Liposarcoma: adipocytes
Rhabdomysaroma: skeletal muscle 
Leiomysaroma: smooth muscle cells 
Chondrsaroma: cartilage 
Ostesarcoma: bone
53
Q

Metastasis

which cancer never metastasises?

A

Malignant tumours spread from their site of origin to form other tumours at distant cites

Basal cell carcinoma NEVER metastasises

54
Q

Bone metastasises from

A

Lung, breast, kidney, thyroid, prostate

55
Q

Carcinomas preferred route

A

Lymphatic spread

56
Q

Sarcoma preferred route

A

Haematogenous spread

57
Q

Define inflammation

A

A local physiological response to injury

58
Q

Most common cause of chronic inflammation

A

Primary chronic inflammation

59
Q

Epitheliod histiocytes

A

Activated macrophages that resemble epithelial cells

Aggregation = granuloma

60
Q

Sarcoidosis

A

Occurs when inflammatory cells clump together to form granulomas

61
Q

Blood marker in the investigation if sarcoidosis

A

Serum ACE

62
Q

Sequence of events in metastasis

A

Invasion: erosion of tissue boundaries

Intravasion: gain access to metastatic routes e.g. lymph

Evasion of host defence

Adherence to endothelium

Extravasation: colonisation of new site

Angiogenesis: develops its own blood supply

63
Q

Primary pulmonary neoplasm to liver, via which spread?

A

Haematogenous spread

64
Q

Bcl-2 role in apoptosis

A

Inhibits apoptosis

65
Q

CO2 reading on an ABG

A

Same direction as pH = metabolic

Opposite direction = respiratory

Belle Phase 2a (14 decks)

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